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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

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PPARγ modulated inflammatory response of human dendritic cell subsets to engulfed apoptotic neutrophils

Gyöngyike Majai1, Péter Gogolák, Csilla Ambrus

  • 1Research Center for Molecular Medicine, University of Debrecen, Egyetem tér 1, Debrecen, Hungary.

Journal of Leukocyte Biology
|August 6, 2010
PubMed

Insights

Human dendritic cells (DCs) show subtype-specific responses to apoptotic neutrophils, influencing immune outcomes. PPARγ activation enhances phagocytosis but not pro-inflammatory or T cell responses, revealing immune modulation mechanisms.

Area of Science:

  • Immunology
  • Cell Biology
  • Innate Immunity

Background:

  • Phagocyte interaction with apoptotic cells critically shapes immune responses.
  • Dendritic cells (DCs) play a key role in initiating adaptive immunity through antigen presentation and cytokine production.

Purpose of the Study:

  • To investigate the phagocytosis of allogeneic, apoptotic neutrophils by human monocyte-derived DCs.
  • To characterize the cytokine profiles and T cell polarization induced by this interaction.
  • To explore the modulatory effects of PPARγ activation on DC responses.

Main Methods:

  • Human monocyte-derived dendritic cells (DCs) and macrophages were used.
  • Phagocytosis assays with allogeneic, apoptotic neutrophils were performed.
  • DC-SIGN function was blocked to assess its role in uptake.
  • Cytokine secretion (IL-8, TNF-α, IL-6, IL-12, IL-10) was measured.
  • T lymphocyte polarization assays were conducted.
  • Peroxisome proliferator-activated receptor gamma (PPARγ) was activated using Rosiglitazone (RSG).

Main Results:

  • Phagocytosis of apoptotic neutrophils by DCs was slower and less efficient than by macrophages.
  • CD1a(-) DCs demonstrated higher phagocytic activity than CD1a(+) DCs.
  • Blocking DC-SIGN partially inhibited apoptotic cell uptake.
  • Interaction with apoptotic neutrophils sensitized DCs to produce pro-inflammatory cytokines (IL-8, TNF-α, IL-6) and Th1-polarizing cytokines (IL-12, IL-10) upon further stimulation.
  • PPARγ activation enhanced phagocytosis but did not augment pro-inflammatory responses or Th1 cell activation capacity of CD1a(-) DCs.

Conclusions:

  • Dendritic cells exhibit subtype-specific inflammatory and T cell responses to allogeneic, apoptotic neutrophils.
  • The anti-inflammatory effects of PPARγ modulate these DC responses, impacting immune outcomes.
  • These findings highlight the complex interplay between apoptotic cell clearance and immune regulation by DCs.

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